Abstract

Introduction: Previous research has suggested that inflammation, oxidative stress, and poor endothelial functioning all have a role in the development of coronary slow flow (CSF). Endothelial dysfunction, atherosclerosis, and microvascular coronary dysfunction have all been linked to inflammation. In this context, uric acid (ÜA) and albumin are hypothesized to be linked to the etiology of coronary slow flow (CSF). The aim of this study was to compare the uric acid to albumin ratios in CSF patients to those in coronary arteries that were angiographically normal. Patients and Methods: 230 patients with CSFP and another 230 people matched for age and gender and confirmed to have normal coronary angiograms participated in a case-control study. Retrospective evaluation of 5500 individuals who underwent coronary angiography at our hospital between January 2015 and August 2020 for known or suspected ischemic heart disease was done in this study. Prior to the coronary angiography, our clinic measures basal UA and albümin. By dividing uric acid by albumin, UA/A was calculated. Thrombolysis in Myocardial Infarction Frame Count was used to measure the CSFP. Results: In order to determine UA/A, üric asid to albümin was divided. UA/A was substantially higher in the CSFP group than in the control group (1.180.21 and 1.50.33, respectively, p0.001). Multiple logistic regression analysis was used to determine whether UA/A predicted independently of CSFP presence. The sensitivity and specificity of the UA/effective A's cut-off points for predicting the presence of CSFP were >1,29 and 81% and 70%, respectively. In comparison to üric asid or albümin alone, UA/A had a higher diagnostic accuracy to predict CSFP (UA AUC:075, albümin AUC:0,552, and ÜA/a AUC:0,826, respectively). Conclusion: We found that patients with CSF had greater levels of UA/A than subjects with normal coronary arteries, This was the first study to show that UA/A was an independent predictor of CSFP.

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